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Unit 6 > GI - from Unit 3 (10.1-10.3 of pathoma) > Flashcards

GI - from Unit 3 (10.1-10.3 of pathoma) Flashcards

1
Q

Cleft lip and palate

A

Full-thickness defect of lip or palate

Due to failure of facial prominences to fuse

Cleft lip and palate usually occur together

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2
Q

What is the usual cause of a cleft lip and palate?

A

Due to failure of facial prominences to fuse

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3
Q

Aphthous Ulcer

A
  • Painful, superifical ulceration of oral mucosa
  • arises in relation to stress and resolves spontaneously, but often recurs
  • characterized by grayish base surrounded by erythema
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4
Q

Behcet Syndrome

A

Presents as a triad

  • recurrent aphthous ulcers
  • genital ulcers
  • uveitis

Due to immune complex vasculitis involving small vessles.

Can be seen after viral infection, but etiology is unknown

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5
Q

Behcet Syndrome - What is it commonly caused by?

A

Due to immune complex vasculitis involving small vessles.

Can be seen after viral infection, but etiology is unknown

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6
Q

Triad associated with Behcet Syndrome

A
  1. recurrent aphthous ulcers
  2. genital ulcers
  3. uveitis
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7
Q

Oral Herpes

A

Vesicles involving oral mucosa that rupture resulting in shallow, painful, red ulcers

Usually due to HSV-1

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8
Q

Most common cause of oral herpes?

A

HSV-1

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9
Q

Oral herpes - how does it infection humans?

A
  • Primary infection occurs in childhood. Lesions heal, but virus remains dormant in ganglia of trigeminal nerve.
  • Stress and sunlight cause reactivation of virus
  • Leads to vesciles that often arise on lips (cold sore)
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10
Q

Where does herpes simple viruses lay dormant in oral herpes?

A

ganglia of trigeminal nerve

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11
Q
A

Oral herpes

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12
Q

Squamous cell carcinoma of the oral mucosa

A

Malignant neoplasm of squamous cells lining oral mucosa

Major risk factors

  • tobacco
  • alcohol

Floor of mouth is most common location

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13
Q

Major risk factors for squamous cell carcinoma of the oral mucosa

A

tobacco

alcohol

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14
Q

Most common location for squamous cell carcinoma of the oral mucosa

A

floor of the mouth

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15
Q

Squamous dysplasia of the oral mucosa - classic presentation

A

Often presents as leukoplakia (white plaques) and erythroplakia (red plaque)

  • biopsied to rule out carcinoma
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16
Q

Patient presents with oral leukoplakia, what 3 things come to mind?

A

Have to distinguish between 3 things:

  1. squamous cell dysplasia – presents as a white plaque that cannot be scraped away
  2. oral candidiasis (thrush) – white deposit on the tongue that is easily scraped away. Usually seen in immunocompromised states
  3. Hairy leukoplakia – white, rough (‘hairy’) patch that arises on the lateral tongue. Usually seen in immunocompromised individuals (AIDS) and is due to EBV-induced squamous cell hyperplasia. NOT premalignant
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17
Q

Erythoplakia of oral mucosa

A

‘Red plaque’

Represents vascularized leukoplakia, ie a lot of new growth that includes angiogenesis

Highly suggestive of squamous cell dysplasia

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18
Q

What is suggestive of squamous dysplasia of oral mucosa?

A

Erythoplakia and leukoplakia.

Erythoplakia is more much indicative that there is dysplasia. Leukoplakia needs to rule out candidiasis and hairy leukoplakia

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19
Q

Major Salivary Glands (3)

A
  1. Parotid
  2. Submandibular
  3. Sublingual
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20
Q

Mumps

A

Infection with mumps virus

results in bilateral inflamed parotid glands

Can also cause

  • orchitis (infection of testicles) –> risk of sterility (teenagers)
  • pancreatitis – will result in increased serum amylase (but need to becareful, because both the gland and the pancreas produce amylase)
  • aseptic meningitis
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21
Q

What other tissues can mumps infect? (besides parotid)

A
  1. orchitis (infection of testicles) –> risk of sterility (teenagers)
  2. pancreatitis – will result in increased serum amylase (but need to becareful, because both the gland and the pancreas produce amylase)
  3. aseptic meningitis
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22
Q

Mumps - why is there an increase in serum amylase?

A

Both overactivity of the infected glands (bilateral parotid) and possible pancreatitis.

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23
Q

Sialadenitis

A

Inflammation of the salivary gland

Most commonly due to an obstruction stone (sialolithiasis) leading to S aureus infection.

  • whenever you block a tube, you increase the likelihood of an infection behind the tube

usually unilateral

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24
Q

sialolithiasis

A

Also termed salivary calculi or salivary stone

A condition where a calcified mass or sialolith forms within a salivary gland, usually in the duct of the submandibular gland

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25
Q

What is the most common cause of sialadenitis? What are you worried about in this case?

A

sialolithiasis which often leads to an S. aureus infection

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26
Q

Pleomorphic adenoma

A
  • Most common tumor of salivary gland
    • Benign tumor composed of stromal (ie cartilage) AND epithelial tissue (ie glands)
  • whenever a tumor comprises of 2 tissues, it is called a biphasic tumor
  • Usually arises in parotid
  • Presents as a mobile, painless, circumscribed mass at angle of jaw
    • all the key characteristics of being benign
      • mobile = did not invade tissue
      • painless = has not invaded the facial nerve (runs right through parotid gland)
      • circumscribed = different from all the tissue surrounding it (hence foreign, but benign)
  • High rate of recurrence
    • mostly due to the fact that this tumor has irregular margins and inexperienced surgeons are more likely to leave a little bit of tissue behind that allows to regrowth
  • Rarely may transform into carcinoma
    • presents with signs of facial nerve damage
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27
Q

Pleomorphic adenoma - most common location

A

Arises in parotid.

Presents as a mobile, painless, circumscribed mass at angle of jaw

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28
Q

Pleomorphic adenoma - classic presentation

A

all the key characteristics of being benign

  • mobile = did not invade tissue
  • painless = has not invaded the facial nerve (runs right through parotid gland)
  • circumscribed = different from all the tissue surrounding it (hence foreign, but benign)
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29
Q

Why is there a high rate of recurrent of pleomorphic adenomas?

A

mostly due to the fact that this tumor has irregular margins and inexperienced surgeons are more likely to leave a little bit of tissue behind that allows to regrowth

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30
Q

Pleomorphic adenoma - what happens when this tumor transforms into a carcinoma? How do you tell?

A

Patients will likely present with pain (invasion/destruction of the facial nerve in the parotid gland)

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31
Q

Warthin tumor

A

Benign cystic tumor with abundant lymphocytes and germinal centers

  • cystic tumor with lymph node tissue

2nd most common tumor of salivary gland

almost always arises in parotid – common for LN tissue to be associated with parotid

32
Q

Warthin tumor - where does it most commonly arise?

A

Parotid gland – this gland is one of the last glands to embryologically separate out and is not uncommon for it to be associated with lymphoid tissue

33
Q

Mucoepidermoid carcinoma

A

Malignant tumor composed of mucinous and squamous cells

Usually arises in parotid; commonly involves the facial nerve (dmg to this nerve is common in malignancies)

34
Q

TE fistula

A

Congenital defect resulting in connection between the esophagus and trachea

multiple different variants, most common: atresia of the proximal esophagus w/ connection of the distal esophagus (other end) to the trachea.

35
Q

TE fistula - classic presentation

A

Presents with:

  • vomiting – food goes into esophagus, but b/c it is closed, it will come right back up
  • excess amniotic fluid (polyhydramnios) – during gestation, baby will “eat” some of the amniotic fluid. Since the esophagus is blocked, baby can’t so will be left with excess amniotic fluid in the sac
  • abdominal distension – air into the stomach (via fistula)
  • aspiration – stomach contents coming back up
36
Q

Esophageal web

A

Thin protrusion of esophageal mucosa, most often in upper mucosa

Presents with dysphagia for poorly chewed food

Increased risk for esophageal squamous cell carcinoma

37
Q

Plummer-Vinson Syndrome

A

Severe iron deficiency anemia

esophageal web

beefy-red tongue due to atrophic glossitis

  • due to atrophy of the mucosa. Redness due to exposure of the underlying vasculature
38
Q

Plummer-Vinson Syndrome: why do patients present with a beefy red tongue?

A

due to atrophy of the mucosa. Redness due to exposure of the underlying vasculature

39
Q

Zenker diverticulum

A

Outpouching of pharyngeal mucosa through acquired defect in the muscular wall

  • typically due to some abnormal pressure in the pharynx when you are swallowing

Arises above upper esophageal sphincter at junction of esophagus and pharynx

Presents with dysphagia, obstruction and halitosis (bad breathe – food trapped can rot)

Also known referred to sometimes as a “false” diverticulum

  • means you only protruded one part of the wall and it does not include the muscularis layer
40
Q

Zenker Diverticulum - classic presentation

A

Presents with dysphagia, obstruction and halitosis (bad breathe – food trapped can rot)

41
Q

False diverticulum

A

A diverticulum that does not include the muscularis or adventitia. Typically very superifical diverticulum.

Most of the GI diverticulums (including Zenker’s) are false diverticulums

42
Q

Mallory-Weiss Syndrome

A

Longitudinal laceration of mucosa at GE junction

Caused by severe vomiting –> which causes a longitudinal laceration of the GE mucosa as the vomit comes up each time.

  • Usually due to alcoholism or bulimia

Presents with painful hematemesis (laceration bleeds into the vomit)

Risk of Boerhaave syndrome

43
Q

Mallory-Weiss Syndrome: classic presentation

A

Presents with painful hematemesis (laceration bleeds into the vomit)

44
Q

Mallory-Weiss Syndrome: What is the cause?

A

Caused by severe vomiting –> which causes a longitudinal laceration of the GE mucosa as the vomit comes up each time.

Usually due to alcoholism or bulimia

45
Q

Boerhaave syndrome

A

Rupture of esophagus, typically occuring after forceful emesis. Associated with but also different than Mallory-Weiss syndrome (which is a nontransmural esophageal tear)

46
Q

Pathogenesis of Boerhaave Syndrome

A

Rupture of esophagus –> air in the mediastinum –> air track up through the facial planes and get into the subcutaneous tissue (esp in region of neck) –> subcutaneous emphysema (air beneath the skin); will get crackling when you press the skin

47
Q

Esophageal varices

A
  • Dilated submucosal veins in lower esophagus
  • Arise secondary to portal HTN (a portion of the blood supply to the esophagus drains into the portal system (the majority going via azygous vein into the SVC))
  • Asymptomatic, but risk of rupture exists (painless hematemesis if ruptured)
  • most common type of death in patients with cirrhosis (who all have portal hypertension, and reduce coagulation factors –> massive bleeding)
48
Q

How do esophageal varices arise?

A

Arise secondary to portal HTN (a portion of the blood supply to the esophagus drains into the portal system (the majority going via azygous vein into the SVC))

49
Q

What is the most common cause of death in patients with cirrhosis? and why?

A

Esophageal varices.

Patients with cirrhosis have malfunctional liver alongside portal hypertension. The portal hypertension predisposes them to esophageal varices that can rupture and the malfunctional liver reduces the production of coagulation factors so any kind of bleed will be amplified with an inability to clot.

50
Q

Achalasia

A

A = without, chalasia = relaxation

Disordered esophageal motility with inability to relax LES

Due to damaged ganglion cells in myenteric plexus (major nerve supply to the GI and responsible for GI tract mobility)

  • dmg can be idiopathic or secondary to known insult (ie Chagas disease – trypanosome infection)
51
Q

myenteric plexus - what is it? what is it for?

A

The myenteric plexus is the major nerve supply to the gastrointestinal tract and controls GI tract motility.

52
Q

2 common symptoms associated with achalasia

A
  1. inability to relax the LES
  2. dysfunctional esophageal motility
53
Q

Achalasia - clinical features

A

3, 4 – Inability to relax the LES –> buildup of food at the LES = increased LES pressure –> expansion of the esophageal walls to accomodate the buildup == bird beak sign

  1. Dysphagia for solids and liquids – both solids and liquids require the peristalsis of the esophageal wall
  2. Putrid breathe - solids accumulates in the esophagus and will rot creating the bad breathe
  3. High LES pressure on esophageal manometry
  4. “bird-beak” sign on barium swallow
  5. Increased risk for esophageal squamous cell carcinoma
54
Q

Why is there a dysphagia for solids and liquids with achalasia?

A

both solids and liquids require the peristalsis of the esophageal wall

achalasia is associated with dysfunction of the esophageal motility

55
Q

Why is a putrid breathe often found on patients with achalsia?

A

solids accumulates in the esophagus and will rot creating the bad breathe

56
Q

GERD

A

Gastroesophageal reflux disease

reflux of acid from the stomach due to reduced LES tone

57
Q

Most common cause of GERD

A

reflux of acid from the stomach due to reduced LES tone

58
Q

GERD - risk factors

A
  • alcohol
  • tabacco
  • obesity
  • fat-rich diet
  • caffeine
  • hiatal hernia (hernia of the stomach into the esophagus which bypasses the LES. W/o the LES, the changes of reflux are significantly higher)
59
Q

GERD - classical clinical features

A
  1. heartburn (mimics cardiac chest pain)
  2. asthma (adult-onset) and cough
  3. damage to enamel of teeth
  4. ulceration with stricture and Barrett esophagus are late complications
60
Q

Normal cellular lining of the esophagus

A

Non-keratinizing squamous epithelium

61
Q

What does the lining of the esophagus change into due to GERD?

A

Non-ciliated columnar cells with goblet cells

62
Q

Sliding hiatal hernia

A

hernia of the stomach into the esophagus which bypasses the LES.

W/o the LES, the changes of reflux are significantly higher –> increased risk for GERD

63
Q

Paraesophageal hernia

A
  • hernia of the stomach through the diaphram alongside the esophagus.
  • Distinguished by having bowel sounds in the lower lung fields.
  • Doesn’t necessarily result in GERD.
64
Q

How do you diagnose paraesophageal hernia in the clinic?

A

Distinguished by having bowel sounds in the lower lung fields.

65
Q
A
66
Q

Barrett esophagus

A

Most commonly associated with GERD

Metaplasia from a non-keratinizing squamous epithelium (NKSE) to a non-ciliated columnar epithelium with goblet cells in the lower 1/3 of the esophagus

  • this is a response of the stem cells to stress
  • b/c it is a metaplasia, it can progress to dysplasia and then henceforth to adenocarcinoma
67
Q

Esophageal carcinoma - 2 major classifications

A

Adenocarcinoma - malignant proliferation of glands

  • normally do not have glands in the esophagus. Requires the metaplasia associated with Barrett’s esophagus that progresses into the adenocarcinoma.
  • This metaplasia only occurs in the lower 1/3 of the esophagus
  • most common type of esophageal carcinoma in the west

Squamous cell carcinoma

  • most common esophageal cancer worldwide
  • usually arises in upper or middle third of the esophagus
  • Risk factors: anything that causes irritation to the esophagus
    • alcohol and tobacco
    • very hot tea (southern china and iran)
    • achalasia (rotting of the food that builds up irritates the mucosa)
    • esophageal web (ie plummer-vinson syndrome) – also via the rotting of food that gets lodged
    • esophageal injury (ie lye ingestion)
68
Q

Esophageal squamous cell carcinoma - risk factors

A

anything that causes irritation to the esophagus

  • alcohol and tobacco
  • very hot tea (southern china and iran)
  • achalasia (rotting of the food that builds up irritates the mucosa)
  • esophageal web (ie plummer-vinson syndrome) – also via the rotting of food that gets lodged
  • esophageal injury (ie lye ingestion)
69
Q

Why is there a high rate of incidence of esophageal carcinoma in southern china and iran? What type of cancer is it?

A

Squamous cell carcinoma.

Due to their habits of drinking hot tea. Hot tea irritates the esophagus and increases the risk of carcinoma

70
Q

Esophageal carcinoma - presentation

A

Presents late

  • Progressive dysphagia (starts as a dysphagia for solids and progresses to dysphagia for solids + liquids as the tumor gets bigger)
  • weight loss
  • pain
  • hematemesis (as the cancer grows, it will expand the mucosa which can result in bleeding and pain)
  • squamous cell carcinoma may additionally present with hoarse voice (invasion into the recurrent laryngeal nerve) and cough (invasion into trachea)
71
Q

Esophageal squamous cell carcinoma - additional symptoms

A

Located in the upper 2/3 of the eosphagus (typically).

may additionally present with hoarse voice (invasion into the recurrent laryngeal nerve) and cough (invasion into trachea)

72
Q

Regional lymph node spreading of esophageal carcinoma

A

Upper 1/3 – cervical nodes

Middle 1/3 – mediastinal or tracheobronchial nodes

Lower 1/3 – celiac and gastric nodes

73
Q

If an esophageal carcinoma arises in the upper 1/3 of the esophagus, which lymph node(s) will the cancer likely spread to?

A

Cervical nodes

74
Q

If an esophageal carcinoma arises in themiddle 1/3 of the esophagus, which lymph node(s) will the cancer likely spread to?

A

mediastinal or tracheobronchial nodes

75
Q

If an esophageal carcinoma arises in the lower 1/3 of the esophagus, which lymph node(s) will the cancer likely spread to?

A

celiac and gastric nodes

76
Q

Neural tube defects - cause and association

A

Arise from incomplete closure of neural tube

Associated with low folate levels prior to conception

Unit 6 (10 decks)

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